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Cell adaptation to activated FGFR3 includes Sprouty4 up regulation to inhibit the receptor-mediated ERKs activation from the endoplasmic reticulum |
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| Authors: | Patricia M-J. Lievens Elena Zanolli Elio Liboi |
| Affiliation: | a Department of Morphological and Biomedical Sciences, Division of Biochemistry, University of Verona Medical School, Verona, Italy b Department of Health Sciences, University of Molise Medical School, Campobasso, Italy c Department of Neuroscience and Brain Technologies, Italian Institute of Technology, Genova, Italy |
| Abstract: | The kinase activity of the thanatophoric dysplasia type II-fibroblast growth factor receptor 3 mutant (TDII-FGFR3) hampers its maturation. As a consequence, the immature receptor activates extracellular regulated kinases (ERKs) from the endoplasmic reticulum (ER), which leads to apoptosis. On the other hand, in stable TDII-FGFR3 cells receptor biosynthesis is restored and ERKs are activated from the cell surface. To identify potential mediators of cell adaptation to the activated receptor we investigated gene products that are differently regulated in TDII and wild-type FGFR3 cells. cDNA representational difference analysis reveals Sprouty4 up regulation in the TDII-FGFR3 cells. Interestingly, Sprouty4 inhibits the TDII-FGFR3-mediated ERKs activation from the ER, but fails to suppress ERKs activation from cell surface. We conclude that cell adaptation to activated FGFR3 include Sprouty4 activity, which silences the premature receptor signaling and suppress apoptosis. |
| Keywords: | FGFR3, fibroblast growth factor receptor 3 TDII, thanatophoric dysplasia type II cDNA-RDA, cDNA representational difference analysis ERK, extracellular regulated kinases ER, endoplasmic reticulum |
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